It has been shown that CIS inhibits GHR-JAK2 activity by two different mechanisms: (1) the initial inhibition, in which a decreased GH-stimulated STAT5β level is stated due to CIS and STAT5β competitive binding to GHR phosphotyrosines or (2) the time-dependent inhibition connected with proteasomal degradation of CIS with accompanied degradation of GHR-JAK2 complex. This evidence concerns the gene GH1 and in situ carcinoma.